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Association of dopamine transporter reduction with psychomotor impairment in methamphetamine abusers.
TLDR
Evidence is provided that methamphetamine at dose levels taken by human abusers of the drug leads to dopamine transporter reduction that is associated with motor and cognitive impairment and the urgency of alerting clinicians and the public of the long-term changes that methamphetamine can induce in the human brain.
Low level of brain dopamine D2 receptors in methamphetamine abusers: association with metabolism in the orbitofrontal cortex.
TLDR
The association between level of dopamine D2 receptors and metabolism in the orbit ofrontal cortex in methamphetamine abusers suggests that D2 receptor-mediated dysregulation of the orbitofrontal cortex could underlie a common mechanism for loss of control and compulsive drug intake in drug-addicted subjects.
Dopamine transporter occupancies in the human brain induced by therapeutic doses of oral methylphenidate.
TLDR
Oral methylphenidate is very effective in blocking dopamine transporters, and at the weight-adjusted doses used therapeutically (0.3 to 0.6 mg/kg), it is likely to occupy more than 50% of the dopamineTransporter.
Association between decline in brain dopamine activity with age and cognitive and motor impairment in healthy individuals.
TLDR
Age-related decreases in brain dopamine activity are associated with a decline in motor function and may also contribute to impaired performance on tasks that involve frontal brain regions, including measures of abstraction and mental flexibility.
Higher cortical and lower subcortical metabolism in detoxified methamphetamine abusers.
TLDR
Evidence is provided that, in humans, methamphetamine abuse results in changes in function of dopamine- and nondopamine-innervated brain regions, and the higher metabolism seen in the parietal cortex is the result of methamphetamine effects in circuits other than those modulated by dopamine.
Is methylphenidate like cocaine? Studies on their pharmacokinetics and distribution in the human brain.
TLDR
It is speculated that because the experience of the high is associated with the fast uptake of cocaine and methylphenidate in the brain, the slow clearance ofethylphenidate from the brain may serve as a limiting factor in promoting its frequent self-administration.
Decreases in dopamine receptors but not in dopamine transporters in alcoholics.
TLDR
Because D2 receptors in striatum are mainly localized in gamma-aminobutyric acid (GABA) cells these results provide evidence of GABAergic involvement in the dopaminergic abnormalities seen in alcoholics.
Reinforcing effects of psychostimulants in humans are associated with increases in brain dopamine and occupancy of D(2) receptors.
TLDR
It is shown that stimulant-induced high, a mood descriptor that reflects reinforcing effects of drugs in humans, is associated with increases in brain dopamine, and also that there is a quantitative relationship between levels of D(2) receptor occupancy by dopamine and the intensity of the high.
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